Results: Treatment of HFD-fed mice with DISGT significantly lowered body weight, liver weight, and the levels of lipids, including total cholesterol, low-density lipoprotein-cholesterol, and triglycerides. Glucose levels were also lowered. In the aorta, DISGT attenuated atherosclerotic lesions and reduced the expression of ICAM-1, VCAM-1, and E-selectin. Moreover, DISGT decreased lipid accumulation, inflammatory responses, and FAS levels, and it activated AMPK and reduced ACC expression in liver tissues.

Conclusions: The beneficial, anti-lipolytic, and anti-inflammatory effects of DISGT were mediated by the AMPK pathway. As a result, the expression of inflammatory factors was reduced. Our data provide evidence that DISGT may have strong therapeutic potential in treating vascular diseases, such as atherosclerosis.

Mentions:
The extent of atherosclerotic lesions in the aorta was determined by isolution analysis, and it was confined to the cross-section of the aortic root. Oli Red O staining was used to detect atherosclerotic plaques. The aortic root lesion area was markedly increased in HFD-fed mice (27.72 ± 2.87 mm2; p < 0.01), and it was significantly reduced by treatment with DISGT or statin (7.24 ± 1.81 mm2 or 11.90 ± 1.07 mm2; p < 0.01) (Fig. 2a and b). As demonstrated by western blot analysis, the expression of ICAM-1, VCAM-1, and E-selectin in HFD-fed mice was significantly increased compared with that in ND-fed mice. In contrast, DISGT- or statin-treated mice showed lower expression levels of ICAM-1, VCAM-1, and E-selectin compared with HFD-fed mice (Fig. 2c), and this decrease by DISGT was statistically significant (Fig. 2d).Fig. 2

Mentions:
The extent of atherosclerotic lesions in the aorta was determined by isolution analysis, and it was confined to the cross-section of the aortic root. Oli Red O staining was used to detect atherosclerotic plaques. The aortic root lesion area was markedly increased in HFD-fed mice (27.72 ± 2.87 mm2; p < 0.01), and it was significantly reduced by treatment with DISGT or statin (7.24 ± 1.81 mm2 or 11.90 ± 1.07 mm2; p < 0.01) (Fig. 2a and b). As demonstrated by western blot analysis, the expression of ICAM-1, VCAM-1, and E-selectin in HFD-fed mice was significantly increased compared with that in ND-fed mice. In contrast, DISGT- or statin-treated mice showed lower expression levels of ICAM-1, VCAM-1, and E-selectin compared with HFD-fed mice (Fig. 2c), and this decrease by DISGT was statistically significant (Fig. 2d).Fig. 2

Results: Treatment of HFD-fed mice with DISGT significantly lowered body weight, liver weight, and the levels of lipids, including total cholesterol, low-density lipoprotein-cholesterol, and triglycerides. Glucose levels were also lowered. In the aorta, DISGT attenuated atherosclerotic lesions and reduced the expression of ICAM-1, VCAM-1, and E-selectin. Moreover, DISGT decreased lipid accumulation, inflammatory responses, and FAS levels, and it activated AMPK and reduced ACC expression in liver tissues.

Conclusions: The beneficial, anti-lipolytic, and anti-inflammatory effects of DISGT were mediated by the AMPK pathway. As a result, the expression of inflammatory factors was reduced. Our data provide evidence that DISGT may have strong therapeutic potential in treating vascular diseases, such as atherosclerosis.